ReviewLearning & memory (Cold Spring Harbor, N.Y.)2014
Learning and behavioral deficits associated with the absence of the fragile X mental retardation protein: what a fly and mouse model can teach us.
Review in Learning & memory (Cold Spring Harbor, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
47 citing papers in PubMed, 91 citations in OpenAlex.
- Article
- Behavioral and molecular insights into anxiety in ube3a and fmr1 zebrafish models of autism spectrum disorders.Translational psychiatry · 2025Article
- Aberrant hippocampal gamma oscillations in a mouse model of fragile X syndrome: insights from in vitro slice models.Molecular autism · 2025Article
- Article
- Activation of the 5-HT1A Receptor by Eltoprazine Restores Mitochondrial and Motor Deficits in aInternational journal of molecular sciences · 2024Article
- Article
- Astroglial Kir4.1 potassium channel deficit drives neuronal hyperexcitability and behavioral defects in Fragile X syndrome mouse model.Nature communications · 2024Article
- Deregulation of ER-mitochondria contact formation and mitochondrial calcium homeostasis mediated by VDAC in fragile X syndrome.Developmental cell · 2023Article
- Review
- Experience-dependent changes in hippocampal spatial activity and hippocampal circuit function are disrupted in a rat model of Fragile X Syndrome.Molecular autism · 2022Article
- A perspective on molecular signalling dysfunction, its clinical relevance and therapeutics in autism spectrum disorder.Experimental brain research · 2022Review
- AAV-delivered diacylglycerol kinase DGKk achieves long-term rescue of fragile X syndrome mouse model.EMBO molecular medicine · 2022Article
- SRF depletion in early life contributes to social interaction deficits in the adulthood.Cellular and molecular life sciences : CMLS · 2022Article
- Increased 2-arachidonoyl-sn-glycerol levels normalize cortical responses to sound and improve behaviors in Fmr1 KO mice.Journal of neurodevelopmental disorders · 2021Article
- Genetic association of FMRP targets with psychiatric disorders.Molecular psychiatry · 2021Article
- Defective memory engram reactivation underlies impaired fear memory recall in Fragile X syndrome.eLife · 2020Article
- BRAG2a Mediates mGluR-Dependent AMPA Receptor Internalization at Excitatory Postsynapses through the Interaction with PSD-95 and Endophilin 3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Deletion of Fmr1 from Forebrain Excitatory Neurons Triggers Abnormal Cellular, EEG, and Behavioral Phenotypes in the Auditory Cortex of a Mouse Model of Fragile X Syndrome.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Mechanisms underlying auditory processing deficits in Fragile X syndrome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Hippocampal deficits in neurodevelopmental disorders.Neurobiology of learning and memory · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Fragile X syndrome (FXS) is the most frequent form of inherited mental disability and is considered a monogenic cause of autism spectrum disorder. FXS is caused by a triplet expansion that inhibits the expression of the FMR1 gene. The gene product, the Fragile X Mental Retardation Protein (FMRP), regulates mRNA metabolism in brain and nonneuronal cells. During brain development, FMRP controls the expression of key molecules involved in receptor signaling, cytoskeleton remodeling, protein synthesis and, ultimately, spine morphology. Symptoms associated with FXS include neurodevelopmental delay, cognitive impairment, anxiety, hyperactivity, and autistic-like behavior. Twenty years ago the first Fmr1 KO mouse to study FXS was generated, and several years later other key models including the mutant Drosophila melanogaster, dFmr1, have further helped the understanding of the cellular and molecular causes behind this complex syndrome. Here, we review to which extent these biological models are affected by the absence of FMRP, pointing out the similarities with the observed human dysfunction. Additionally, we discuss several potential treatments under study in animal models that are able to partially revert some of the FXS abnormalities.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.